Williams Obstetrics, 24th Edition

CHAPTER 47. Critical Care and Trauma








An endless number of medical, surgical, and obstetrical complications may be encountered in pregnancy or the puerperium. Those that are more complex and life threatening can be particularly challenging, especially when a multidisciplinary team is necessary for optimal care. It is axiomatic that obstetricians and other members of the health-care team have a working knowledge of the unique considerations for pregnant women. Some of those discussed in Chapter 46 include pregnancy-induced physiological changes, alterations in normal laboratory values, and finally and importantly, consideration for the second patient—the fetus. Because these severely ill women are usually young and in good health, their prognosis is generally better than that of many other patients admitted to intensive care units.


In the United States each year, 1 to 3 percent of pregnant women require critical care services, and the risk of death during such admission ranges from 2 to 11 percent (American Academy of Pediatrics and the American College of Obstetricians and Gynecologists, 2012). Those with pregnancy-associated complications—especially hemorrhage and hypertension—have the greatest need for intensive care (Baskett, 2009; Kuklina, 2009; Madan, 2008). That said, many antepartum admissions are for nonobstetrical reasons, and in our experiences from Parkland Hospital, these include diabetes, pneumonia or asthma, heart disease, chronic hypertension, pyelonephritis, or thyrotoxicosis (Zeeman, 2006). In addition to antenatal treatment, intrapartum and postpartum critical care for hypertensive disorders, hemorrhage, sepsis, or cardiopulmonary complications may be required for many. In instances of life-threatening hemorrhage, surgical procedures may be necessary, and close proximity to a delivery-operating room is paramount. For women who are undelivered, fetal well-being is also better served by this close proximity.

image Organization of Critical Care

The concept and development of critical care for all aspects of medicine and surgery began in the 1960s. The National Institutes of Health held a Consensus Conference (1983) and the Society of Critical Care Medicine (1988, 1999) subsequently established guidelines for intensive care units (ICUs). Especially pertinent to obstetrics, costly ICUs prompted evolution of a step-down intermediate care unit. These units were designed for patients who did not require intensive care, but who needed a higher level of care than that provided on a general ward. The American College of Critical Care Medicine and the Society of Critical Care Medicine (1998) published guidelines for these units (Table 47-1).

TABLE 47-1. Guidelines for Conditions That Could Qualify for Intermediate Care

Cardiac: evaluation for possible infarction, stable infarction, stable arrhythmias, mild-to-moderate congestive heart failure, hypertensive urgency without end-organ damage

Pulmonary: stable patients for weaning and chronic ventilation, patients with potential for respiratory failure who are otherwise stable

Neurological: stable central nervous system, neuromuscular, or neurosurgical conditions that require close monitoring

Drug overdose: hemodynamically stable

Gastrointestinal: stable bleeding, liver failure with stable vital signs

Endocrine: diabetic ketoacidosis, thyrotoxicosis that requires frequent monitoring

Surgical: postoperative from major procedures or complications that require close monitoring

Miscellaneous: early sepsis, patients who require closely titrated intravenous fluids, pregnant women with severe preeclampsia or other medical problems

From Nasraway, 1998.

image Obstetrical Critical Care

Although the evolution of critical care for obstetrical patients has generally followed developments described above, there are no specific guidelines. Most hospitals employ a blend of these concepts, and in general, units can be divided into three types.

1. Medical or Surgical ICU—in most hospitals, severely ill women are transferred to a unit operated by medical and surgical “intensivists.” Admissions or transfers to these units are situation-specific and based on the acuity of care needed and on the ability of the facility to provide it. For example, in most institutions, pregnant women who require ventilatory support, invasive monitoring, or pharmacological support of circulation are transferred to an ICU. Another example is the neurological ICU (Sheth, 2012). A review of more than 25 tertiary-care referral institutions indicated that approximately 0.5 percent of obstetrical patients are transferred to these types of ICUs (Zeeman, 2006).

2. Obstetrical Intermediate Care Unit—sometimes referred to as a High-Dependency Care Unit (HDU)—an example of this system is the one at Parkland Hospital. Located within the labor and delivery unit, it has designated rooms and experienced personnel. The two-tiered system incorporates the guidelines for intermediate and intensive care. Care is provided by maternal-fetal medicine specialists and nurses with experience in critical care obstetrics. As needed, this team is expanded to include other obstetricians and anesthesiologists, gynecological oncologists, pulmonologists, cardiologists, surgeons, and other medical and surgical subspecialists. Many tertiary-care centers have developed similar intermediate care units and use selected triage to ICUs. Guidelines for such transfers must follow the federal Emergency Medical Treatment and Labor Act (EMTALA) guidelines. According to the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2012), the minimal monitoring required for a critically ill patient during transport includes continuous pulse oximetry, electrocardiography, and regular assessment of vital signs. All critically ill patients must have secure venous access before transfer. Those who are mechanically ventilated must have their endotracheal tube position confirmed and secured before transfer. Left uterine displacement and supplemental oxygen should be applied routinely during transport of antepartum patients. The utility of continuous fetal heart rate or tocodynamic monitoring is unproven, therefore, its use should be individualized.

3. Obstetrical Intensive Care Unit—these units are full-care ICUs as described above, but are operated by obstetrical and anesthesia personnel in the labor and delivery unit. Very few units have these capabilities (Zeeman, 2003, 2006).

For smaller hospitals, transfer to a medical or surgical ICU may be preferable, and sometimes transfer to another hospital is necessary. As discussed, indications for admission to these various types of critical care units are highly variable. Shown in Table 47-2 are some examples. The American College of Obstetricians and Gynecologists (2011a) has summarized critical obstetrical care implementation depending on hospital size and technical facilities. Somewhat related, the concept has been explored of a medical emergency team—MET—for rapid response to emergent obstetrical situations (Gosman, 2008).

TABLE 47-2. Comparison of Acuity of Patient Mix for Obstetrical Critical Care Shown in Percent


image Pulmonary Artery Catheter

Data obtained during pregnancy with the pulmonary artery catheter (PAC) have contributed immensely to the understanding of normal pregnancy hemodynamics and pathophysiology of common obstetrical conditions. These include preeclampsia-eclampsia, acute respiratory distress syndrome (ARDS), and amnionic-fluid embolism (Clark, 1988, 1995, 1997; Cunningham, 1986, 1987; Hankins, 1984, 1985). Because of these studies, most have concluded that such monitoring is seldom necessary (American College of Obstetricians and Gynecologists, 2013; Dennis, 2012).

In nonobstetrical patients, randomized trials of nearly 5000 subjects have shown no benefits with pulmonary artery catheter monitoring (Harvey, 2005; Richard, 2003; Sandham, 2003). A randomized trial by the National Heart, Lung, and Blood Institute (2006b) assessed catheter-guided therapy in 1000 patients with ARDS. Invasive monitoring did not improve outcomes and had more complications. According to a recent Cochrane Database review, there have been no randomized trials using this for preeclampsia management (Li, 2012). Overall mechanisms, benefits, and risks were reviewed by Vincent (2011).

image Hemodynamic Changes in Pregnancy

Formulas for deriving some hemodynamic parameters are shown in Table 47-3. These measurements can be corrected for body size by dividing by body surface area (BSA) to obtain index values. Normal values for nonpregnant adults are used but with the caveat that these may not necessarily reflect changes induced by more “passive” uteroplacental perfusion (Van Hook, 1997).

TABLE 47-3. Formulas for Deriving Various Cardiopulmonary Parameters

Mean arterial pressure (MAP) (mm Hg) = [SBP + 2 (DBP)] ÷ 3

Cardiac output (CO) (L/min) = heart rate × stroke volume

Stroke volume (SV) (mL/beat) = CO/HR

Stroke index (SI) (mL/beat/m2) = stroke volume/BSA

Cardiac index (CI) (L/min/m2) = CO/BSA

Systemic vascular resistance (SVR) (dynes × sec × cm−5) = [(MAP − CVP)/CO] × 80

Pulmonary vascular resistance (PVR) (dynes × sec × cm−5) = [(MPAP − PCWP)/CO] × 80

BSA = body surface area (m2); CO = cardiac output (L/min); CVP = central venous pressure (mm Hg); DBP = diastolic blood pressure; HR = heart rate (beats/min); MAP = mean systemic arterial pressure (mm Hg); MPAP = mean pulmonary artery pressure (mm Hg); PCWP = pulmonary capillary wedge pressure (mm Hg); SBP = systolic blood pressure.

In a landmark investigation, Clark and colleagues (1989) used pulmonary artery catheterization to obtain cardiovascular measurements in healthy pregnant women and again in these same women when nonpregnant. These values are shown in Chapter 4 (Table 4-4p. 60) and are also plotted on a ventricular function curve (Fig. 4-9p. 59). Because increased blood volume and cardiac output are compensated by decreased vascular resistance and increased pulse rate, ventricular performance remains within the normal range at term. A working knowledge of these changes is paramount to understanding the pathophysiology of pregnancy complications discussed later in this chapter and throughout the book.


The incidence of pulmonary edema complicating pregnancy averages 1 in 500 to 1000 deliveries at tertiary referral centers. The two general causes are: (1) cardiogenic—hydrostatic edema caused by high pulmonary capillary hydraulic pressures and (2) noncardiogenic—permeability edema caused by capillary endothelial and alveolar epithelial damage. In pregnancy, noncardiogenic pulmonary edema is more common. Taken in toto, studies in pregnant women indicate that more than half who develop pulmonary edema have some degree of sepsis syndrome in conjunction with tocolysis, severe preeclampsia, or obstetrical hemorrhage combined with vigorous fluid therapy (Thornton, 2011). To categorize these differences, Dennis and Solnordal (2012) proposed a classification to include those women who are normotensive or hypotensive versus those with hypertension.

Although cardiogenic pulmonary edema is less frequent, common precipitating causes include resuscitation for hemorrhage and vigorous treatment of preterm labor. The causes in 51 women with pulmonary edema were cardiac failure, tocolytic therapy, iatrogenic fluid overload, or preeclampsia, approximately a fourth each (Sciscione, 2003). In another study, more than half of cases were associated with preeclampsia, and there was equal distribution of the other three causes (Hough, 2007). Although used less commonly today, tocolytic therapy with β-mimetic drugs at one time was the cause of up to 40 percent of pulmonary edema cases (DiFederico, 1998; Jenkins, 2003).

image Noncardiogenic Increased Permeability Edema

Endothelial activation is the common denominator that is associated with preeclampsia, sepsis syndrome, and acute hemorrhage—or frequently combinations thereof—and they are the most common predisposing factors to pulmonary edema (Table 47-4). As discussed, these clinical scenarios are often associated with corticosteroids given to hasten fetal lung maturation along with vigorous fluid replacement and tocolytic therapy (Thornton, 2011). Although parenteral β-agonists are undisputedly linked to pulmonary edema, indictment of magnesium sulfate is less convincing. In one study in which pulmonary edema developed in 8 percent of nearly 800 women given magnesium sulfate for preterm labor, half of these were also given terbutaline (Samol, 2005). In our extensive experiences at Parkland Hospital with the use of magnesium sulfate for neuroprophylaxis for severe preeclampsia, we remain dubious that magnesium per se causes pulmonary edema. Similar conclusions were reached following a review by Martin and Foley (2006).

TABLE 47-4. Some Causes and Associated Factors for Pulmonary Edema in Pregnancy

Noncardiogenic permeability edema—endothelial activation with capillary-alveolar leakage:

Preeclampsia syndrome

Acute hemorrhage

Sepsis syndrome

Tocolytic therapy—β-mimetics, MgSO4

Aspiration pneumonitis

Vigorous intravenous fluid therapy

Cardiogenic pulmonary edema—myocardial failure with hydrostatic edema from excessive pulmonary capillary pressure:

Hypertensive cardiomyopathy

Obesity—adipositas cordis

Left-sided valvular disease

Vigorous intravenous fluid therapy

image Cardiogenic Hydrostatic Edema

Ventricular failure causing pulmonary edema in pregnancy is usually associated with some form of gestational hypertension. Although it can be due to congenital or acquired anatomical defects, diastolic dysfunction is frequently from chronic hypertension, obesity, or both (Jessup, 2003; Kenchaiah, 2002). In these women, acute systolic hypertension exacerbates diastolic dysfunction and causes pulmonary edema (Dennis, 2012; Gandhi, 2001). Of note, concentric and eccentric hypertrophy is two- to threefold more common in black women compared with white women (Drazner, 2005).

Despite an underlying cardiomyopathy, heart failure is commonly precipitated by preeclampsia, hypertension, hemorrhage and anemia, and puerperal sepsis (Cunningham, 1986; Sibai, 1987). In many of these, when echocardiography is done later, systolic function is normal as measured by ejection fraction, but evidence for diastolic dysfunction can often be found (Aurigemma, 2004). The use of brain natriuretic peptide (BNP) has not been evaluated extensively in pregnancy (Chap. 4p. 61 and Appendixp. 1291). This neurohormone is secreted from ventricle myocytes and fibroblasts with distention seen in heart failure. In nonpregnant patients, values < 100 pg/mL have an excellent negative-predictive value, and levels > 500 pg/mL have an excellent positive-predictive value. It is problematic that levels frequently are 100 to 500 pg/mL, and thus nondiagnostic (Ware, 2005). Values for N-terminal BNP and atrial natriuretic peptide (ANP) are both elevated with preeclampsia (Tihtonen, 2007).

image Management

Acute pulmonary edema requires emergency management. Furosemide is given in 20- to 40-mg intravenous doses along with therapy to control dangerous hypertension. Further treatment depends on whether a woman is ante- or postpartum and whether the fetus is alive or not. A live fetus prohibits the use of cardioactive drugs that might lower peripheral resistance and in turn severely diminish uteroplacental circulation. The cause of cardiogenic failure is determined by echocardiography, which will help direct further therapy. Acute pulmonary edema is not, per se, an indication for emergency cesarean delivery. Indeed, in most cases, these women are better served by vaginal delivery.


Acute lung injury that causes a form of severe permeability pulmonary edema and respiratory failure is termed acute respiratory distress syndrome (ARDS). This is a pathophysiological continuum from mild pulmonary insufficiency to dependence on high inspired oxygen concentrations and mechanical ventilation. Because there are no uniform criteria for its diagnosis, the incidence is variably reported. One review computed it to be 1 in 3000 to 6000 deliveries, and this comports with our experiences at Parkland Hospital (Catanzarite, 2001). In its most extreme form requiring ventilatory support, there is an associated mortality rate of 45 percent. This rate can be as high as 90 percent if caused or complicated by sepsis (Phua, 2009). Although they are younger and usually healthier than the overall population, pregnant women still have mortality rates of 25 to 40 percent (Catanzarite, 2001; Cole, 2005). Finally, if ARDS develops antepartum, there is a correspondingly high perinatal mortality rate.

image Definitions

Physiological criteria required for diagnosis of acute respiratory distress syndrome are study dependent. In general, less precise terms are used for clinical care. Most investigators have defined ARDS as radiographically documented pulmonary infiltrates, a ratio of arterial oxygen tension to the fraction of inspired oxygen (Pao2:Fio2) < 200, and no evidence of heart failure (Mallampalli, 2010). Recently, the international consensus-revised Berlin Definition was reported by the ARDS Definition Task Force (2012). It describes categories of mild (200 mm Hg < Pao2/Fio2 ≤ 300 mm Hg); moderate (100 mm Hg < Pao2/Fio2 ≤ 200 mm Hg); and severe (Pao2/Fio2 ≤ 100 mm Hg). To date, for most interventional studies, however, a working diagnosis of acute lung injury is made when the Pao2:Fio2 ratio is < 300 along with dyspnea, tachypnea, oxygen desaturation, and radiographic pulmonary infiltrates (Wheeler, 2007).

image Etiopathogenesis

ARDS is a pathophysiological description that begins with acute lung injury from various causes. Several disorders have been implicated as causes of acute pulmonary injury and permeability edema during pregnancy (Table 47-5). Although many are coincidental, some are more common in pregnant women. For example, in nonpregnant patients, sepsis and diffuse infectious pneumonia are the two most common single-agent causes and together account for 60 percent of cases. In pregnancy, however, pyelonephritis, chorioamnionitis, and puerperal pelvic infection are the most frequent causes of sepsis. As discussed previously, severe preeclampsia and obstetrical hemorrhage are also commonly associated with permeability edema. Importantly, more than half of pregnant women with acute respiratory distress syndrome have some combination of sepsis, shock, trauma, and fluid overload. With acute hemorrhage, the contribution of transfusion-related acute lung injury (TRALI) is unclear in obstetrical patients (Kopko, 2002). This entity is discussed further in Chapter 41 (p. 818).

TABLE 47-5. Some Causes of Acute Lung Injury and Respiratory Failure in Pregnant Women

Pneumonia—bacterial, viral, aspiration

Sepsis syndrome—chorioamnionitis, pyelonephritis, puerperal infection, septic abortion

Hemorrhage—shock, massive transfusion, transfusion-related acute lung injury (TRALI)

Preeclampsia syndrome

Tocolytic therapy

Embolism—amnionic fluid, trophoblastic disease, air, fat

Connective-tissue disease

Substance abuse

Irritant inhalation and burns


Drug overdose

Fetal surgery


Sickle-cell disease

Miliary tuberculosis

From Catanzarite, 2001; Cole, 2005; Golombeck, 2006; Jenkins, 2003; Lapinsky, 2005; Martin, 2006; Oram, 2007; Sheffield, 2005; Sibai, 2014; Zeeman, 2003, 2006.

Endothelial injury in the lung capillaries releases cytokines that recruit neutrophils to the site of inflammation. Here, they elaborate more cytokines to worsen tissue injury. There are three stages of ARDS development. First, the exudative phase follows widespread injury to microvascular endothelium, including the pulmonary vasculature, and there is also alveolar epithelial injury. These result in increased pulmonary capillary permeability, surfactant loss or inactivation, diminished lung volume, and vascular shunting with resultant arterial hypoxemia. Next, the fibroproliferative phase usually begins 3 to 4 days later and lasts up to day 21. Last, the fibrotic phase results from healing, and despite this, the long-term prognosis for pulmonary function is surprisingly good (Herridge, 2003; Levy, 2012).

image Clinical Course

With pulmonary injury, the clinical condition depends largely on the insult magnitude, the ability to compensate for it, and the disease stage. For example, soon after the initial injury, there commonly are no physical findings except perhaps hyperventilation. And at first, arterial oxygenation usually is adequate. Pregnancy-induced mild metabolic alkalosis may be accentuated by hyperventilation. With worsening, clinical and radiological evidence for pulmonary edema, decreased lung compliance, and increased intrapulmonary blood shunting become apparent. Progressive alveolar and interstitial edema develop with extravasation of inflammatory cells and erythrocytes.

Ideally, pulmonary injury is identified at this early stage, and specific therapy is directed at the insult if possible. Further progression to acute respiratory failure is characterized by marked dyspnea, tachypnea, and hypoxemia. Additional lung volume loss results in worsening of pulmonary compliance and increased shunting. There are now diffuse abnormalities by auscultation, and a chest radiograph characteristically demonstrates bilateral lung involvement (Fig. 47-1). At this phase, the injury ordinarily would be lethal in the absence of high inspired-oxygen concentrations and positive airway pressure by mask or by intubation. When shunting exceeds 30 percent, severe refractory hypoxemia develops along with metabolic and respiratory acidosis that can result in myocardial irritability, dysfunction, and cardiac arrest.


FIGURE 47-1 Anteroposterior chest radiograph of a second-trimester pregnant woman with marked bilateral parenchymal and pleural opacification secondary to acute respiratory distress syndrome (ARDS).

image Management

In cases of severe acute lung injury, attempts are made to provide adequate oxygenation of peripheral tissues while ensuring that therapeutic maneuvers do not further aggravate lung injury. At least intuitively, increasing oxygen delivery should produce a corresponding increase in tissue uptake, but this is difficult to measure (Evans, 1999). Support of systemic perfusion with intravenous crystalloid and blood is imperative. As discussed on page 941, the trial conducted by the National Heart, Lung, and Blood Institute (2006b) showed that pulmonary artery catheterization did not improve outcomes. Because sepsis is commonplace in lung injury, vigorous antimicrobial therapy is given for infection, along with debridement of necrotic tissues. Oxygen delivery can be greatly improved by correction of anemia—each gram of hemoglobin carries 1.25 mL of oxygen when 90-percent saturated. By comparison, increasing the arterial Po2 from 100 to 200 mm Hg results in the transport of only 0.1 mL of additional oxygen for each 100 mL of blood.

Reasonable goals in caring for the woman with severe lung injury are to attain a Pao2 of 60 mm Hg or 90-percent saturation at an inspired oxygen content of < 50 percent and with positive end-expiratory pressures < 15 mm Hg. With regard to the pregnancy, it remains controversial whether delivery of the fetus improves maternal oxygenation (Cole, 2005; Mallampalli, 2010).

Mechanical Ventilation

Positive pressure ventilation by face mask may be effective in some women in early stages of pulmonary insufficiency (Roy, 2007). In an attempt to maximize the fetal environment, early intubation is preferred in the pregnant woman if respiratory failure is more likely than not, and especially if it appears imminent. There are many successful formulas for mechanical ventilation management (Levy, 2012). High-frequency oscillation ventilation (HFOV) has not been shown effective in ARDS (Ferguson, 2013; Slutsky, 2013; Young, 2013). Adjustments are made to obtain a Pao2 > 60 mm Hg or a hemoglobin saturation of ≥ 90 percent and a Paco2 of 35 to 45 mm Hg. Lower levels for Pao2 should be avoided, because placental perfusion may be impaired (Levinson, 1974).

For women who require ventilation for any length of time, the maternal mortality rate is approximately 20 percent. In a study of 51 such women, of whom almost half had severe preeclampsia, most required intubation postpartum. Eleven were delivered while being ventilated, and another six were discharged undelivered (Jenkins, 2003). There were two maternal deaths, including a woman who died as a complication of tocolytic treatment. In two other reports, maternal mortality rates were 17 and 25 percent (Chen, 2003; Schneider, 2003). None of these investigators concluded that delivery improved maternal outcome.

Positive End-Expiratory Pressure. With severe lung injury and high intrapulmonary shunt fractions, it may not be possible to provide adequate oxygenation with usual ventilatory pressures, even with 100-percent oxygen. Positive end-expiratory pressure is usually successful in decreasing the shunt by recruiting collapsed alveoli. At low levels of 5 to 15 mm Hg, positive pressure can typically be used safely. At higher levels, impaired right-sided venous return can result in decreased cardiac output, decreased uteroplacental perfusion, alveolar overdistention, falling compliance, and barotrauma (Slutsky, 2013).

Extracorporeal Membrane Oxygenation

As discussed in Chapter 33 (p. 638), extracorporeal membrane oxygenation (ECMO) has been successfully used for neonatal meconium aspiration syndrome. Preliminary observation suggests that it may be useful in adults (Brodie, 2011; Levy, 2012; Peek, 2009). ECMO has been used in pregnant women. In one study, 12 women with influenza-induced lung failure were treated with ECMO, and of four maternal deaths, three were due to anticoagulation-related hemorrhage (Nair, 2011). In other reports, ECMO was used to allow time for lung healing in five pregnant women, and the duration of support in the four survivors was 2 to 28 days (Cunningham, 2006). Technical aspects of ECMO were recently reviewed by Brodie and Bacchetta (2011).

Fetal Oxygenation

The propensity of the hemoglobin molecule to release oxygen is described by the oxyhemoglobin dissociation curve (Fig. 47-2). For clinical purposes, the curve can be divided into an upper oxygen association curve representing the alveolar-capillary environment and a lower oxygen dissociation portion representing the tissue-capillary environment. Shifts of the curve have their greatest impact at the steep portion because they affect oxygen delivery. A rightward shift is associated with decreased hemoglobin affinity for oxygen and hence increased tissue-capillary oxygen interchange. Rightward shifts are produced by hypercapnia, metabolic acidosis, fever, and increased 2,3-diphosphoglycerate levels. During pregnancy, the erythrocyte concentration of 2,3-diphosphoglycerate is increased by approximately 30 percent. This favors oxygen delivery to both the fetus and maternal peripheral tissues (Rorth, 1971).


FIGURE 47-2 Oxyhemoglobin dissociation curve. With higher oxygen tension (Pao2) in the pulmonary alveoli, adult hemoglobin is maximally saturated compared with that at the lower oxygen tension in the tissue capillaries. Note that at any given oxygen tension, fetal hemoglobin carries more oxygen than adult hemoglobin, as indicated by percent saturation.

Fetal hemoglobin has a higher oxygen affinity than adult hemoglobin. As seen in Figure 47-2, its curve is positioned to the left of the adult curve. To achieve 50-percent hemoglobin saturation in the mother, the Pao2 must be 27 mm Hg compared with only 19 mm Hg in the fetus. Under normal physiological conditions, the fetus is constantly on the dissociation, or tissue, portion of the curve. Even with severe maternal lung disease and very low Pao2 levels, oxygen displacement to fetal tissues is favored. Another example of this comes from pregnant women who live at high altitudes, where despite a maternal Pao2of only 60 mm Hg, the fetal Pao2 is equivalent to that of fetuses at sea level (Subrevilla, 1971).

Intravenous Fluids

Although mortality outcomes are similar, conservative versus liberal fluid management is associated with fewer days of mechanical ventilation (Wiedemann, 2006). There are some pregnancy-induced physiological changes that predispose to a greater risk of permeability edema from vigorous fluid therapy. Colloid oncotic pressure (COP) is determined by serum albumin concentration—1 g/dL exerts approximately 6 mm Hg pressure. As discussed in Chapter 4 (p. 67), serum albumin concentrations normally decrease in pregnancy. This results in a decline in oncotic pressure from 28 mm Hg in the nonpregnant woman to 23 mm Hg at term and to 17 mm Hg in the puerperium (Benedetti, 1979; Dennis, 2012). With preeclampsia, endothelial activation with leakage causes extravascular albumin loss and decreased serum albumin levels. As a result in these cases, oncotic pressure averages only 16 mm Hg antepartum and 14 mm Hg postpartum (Zinaman, 1985). These changes have a significant clinical impact on the colloid oncotic pressure/wedge pressure gradient. Normally, this gradient exceeds 8 mm Hg, however, when it is 4 mm Hg or less, there is an increased risk for pulmonary edema. These associations were recently reviewed by Dennis and Solnordal (2012).

image Other Therapy

There were no benefits from artificial or replacement surfactant therapy in 725 nonpregnant patients with sepsis-induced lung failure (Anzueto, 1996). Although inhalation of nitric oxide was found to cause early improvement, mortality rates were unchanged in two studies (Taylor, 2004; Wheeler, 2007). In a trial conducted by the National Heart, Lung, and Blood Institute (2006a), prolonged methylprednisolonetherapy did not reduce mortality rates.

image Long-Term Outcomes

There are no long-term follow-up studies of pregnant women who recover from respiratory distress syndrome. In nonpregnant subjects, there are significant risks for impaired global cognitive function at 3 and 12 months (Pandharipande, 2013). Data from nonpregnant patients indicate a 1- to 2-year hiatus before basic normal activity is restored in all. In a 5-year follow-up study, Herridge and associates (2011) reported normal lung function but significant exercise limitation, physical and psychological sequelae, decreased physical quality of life, and increased costs and use of health-care services.


Sepsis is derived from the ancient Greek sepein, “to rot.” The sepsis syndrome is induced by a systemic inflammatory response to bacteria or viruses or their by-products such as endotoxins or exotoxins. The severity of the syndrome is a continuum or spectrum (Fig. 47-3). Infections that most commonly cause the sepsis syndrome in obstetrics are pyelonephritis (Chap. 53p. 1054), chorioamnionitis and puerperal sepsis (Chap. 37p. 683), septic abortion (Chap. 18p. 356), and necrotizing fasciitis (Chap. 37p. 686). The mortality rate in nonpregnant patients is 20 to 35 percent with severe sepsis and 40 to 60 percent with septic shock (Angus, 2013; Munford, 2012). Mabie and coworkers (1997) reported a 28-percent mortality rate in 18 pregnant women with sepsis and shock. That said, the maternal mortality risk from sepsis is significantly underestimated (Acosta, 2013).


FIGURE 47-3 The sepsis syndrome begins with a systemic inflammatory response syndrome (SIRS) in response to infection that may progress to septic shock.

image Etiopathogenesis

Most of what is known concerning sepsis pathogenesis comes from study of lipopolysaccharide—LPS or endotoxin (Munford, 2012). The lipid A moiety is bound by mononuclear blood cells, becomes internalized, and stimulates release of mediators and a series of complex downstream perturbations. Clinical aspects of the sepsis syndrome are manifest when cytokines are released that have endocrine, paracrine, and autocrine effects (Angus, 2013).

Although the sepsis syndrome in obstetrics may be caused by several pathogens, most cases represent a small group. For example, pyelonephritis complicating pregnancy caused by Escherichia coli and Klebsiella species commonly is associated with bacteremia and sepsis syndrome (Cunningham, 1987; Mabie, 1997). And although pelvic infections are usually polymicrobial, bacteria that cause severe sepsis syndrome are frequently endotoxin-producing Enterobacteriaceae, most commonly E coli. Other pelvic pathogens are aerobic and anaerobic streptococci, Bacteroides species, and Clostridium species. Some strains of group A β-hemolytic streptococci and Staphylococcus aureus—including community-acquired methicillin-resistant strains (CA-MRSA)—produce a superantigen that activates T cells to rapidly cause all features of the sepsis syndrome—toxic shock syndrome(Moellering, 2011; Soper, 2011). This is discussed further in Chapter 37 (p. 690).

There are also potent bacterial exotoxins that can cause severe sepsis syndrome. Examples include exotoxins from Clostridium perfringens, toxic-shock-syndrome toxin-1 (TSST-1) from S aureus, and toxic shock-like exotoxin from group A β-hemolytic streptococci (Daif, 2009; Soper, 2011). These last exotoxins cause rapid and extensive tissue necrosis and gangrene, especially of the postpartum uterus, and may cause profound cardiovascular collapse and maternal death (Nathan, 1993; Sugiyama, 2010). In a review discussed subsequently, the maternal mortality rate from these infections was 58 percent (Yamada, 2010).

Thus, the sepsis syndrome begins with an inflammatory response that is directed against microbial endotoxins and exotoxins (Angus, 2013). CD4 T cells and leukocytes are stimulated to produce proinflammatory compounds that include tumor necrosis factor-α (TNF-α), several interleukins, other cytokines, proteases, oxidants, and bradykinin that result in a “cytokine storm” (Que, 2005; Russell, 2006). Many other cellular reactions then follow that include stimulation of pro- and antiinflammatory compounds, procoagulant activity, gene activation, receptor regulation, and immune suppression (Filbin, 2009; Moellering, 2011). It is also likely that IL-6 mediates myocardial suppression (Pathan, 2004).

The pathophysiological response to this cascade is selective vasodilation with maldistribution of blood flow. Leukocyte and platelet aggregation cause capillary plugging. Worsening endothelial injury causes profound permeability capillary leakage and interstitial fluid accumulation (Fig. 47-4). Depending on the degree of injury and inflammatory response, there is a pathophysiological and clinical continuum as depicted in Figure 47-3. The clinical syndrome begins with subtle signs of sepsis from infection and terminates with septic shock, which is defined by hypotension unresponsive to intravenous hydration. In its early stages, clinical shock results primarily from decreased systemic vascular resistance that is not compensated fully by increased cardiac output. Hypoperfusion results in lactic acidosis, decreased tissue oxygen extraction, and end-organ dysfunction that includes acute lung and kidney injury.


FIGURE 47-4 Endothelial permeability. The normal interendothelial interface is shown in the left inset. Cytokines and other inflammatory mediators disassemble the cellular junctions, resulting in microvascular leaks (right). (Modified from Lee, 2010.)

image Clinical Manifestations

The sepsis syndrome has myriad clinical manifestations that, at least in part, are dependent on the specific invading microorganism and its particular endo- or exotoxins. Some of the general effects of LPS are as follows:

1. Central nervous system: confusion, somnolence, coma, combativeness, fever, or hypoxemia

2. Cardiovascular: tachycardia, hypotension

3. Pulmonary: tachypnea, arteriovenous shunting with dysoxia and hypoxemia, exudative infiltrates from endothelial-alveolar damage, pulmonary hypertension

4. Gastrointestinal: gastroenteritis—nausea, vomiting, and diarrhea; hepatocellular necrosis—jaundice, hyperglycemia

5. Renal: prerenal oliguria, acute kidney injury

6. Hematological: leukocytosis or leukopenia, thrombocytopenia, activation of coagulation with disseminated intravascular coagulation

7. Cutaneous: acrocyanosis, erythroderma, bullae, digital gangrene.

Thus, although capillary leakage initially causes hypovolemia, if intravenous crystalloid is given at this point, then sepsis hemodynamically can be described as a high cardiac output, low systemic vascular resistance condition (Fig. 47-5). Concomitantly, pulmonary hypertension develops, and despite the high cardiac output, severe sepsis likely also causes myocardial depression (Ognibene, 1988). This is often referred to as the warm phase of septic shock. These findings are the most common cardiovascular manifestations of early sepsis, but they can be accompanied by some of the other clinical or laboratory aberrations listed above.


FIGURE 47-5 Hemodynamic effects of sepsis syndrome. Values for normal women at term are shown by dots. With early sepsis, there is high cardiac output and low vascular resistance. With fluid resuscitation, cardiac output increases even more, but so does capillary hydraulic pressure. With continued sepsis, there may be myocardial depression to further increase capillary hydraulic pressure. Decreased plasma oncotic pressure (serum albumin [g] × 6 mm Hg) contributes to interstitial lung fluid and endo/epithelial leak causes alveolar flooding. LVSWI = left ventricular stroke work index; PCWP = pulmonary capillary wedge pressure.

The response to initial intravenous hydration may be prognostic. Most pregnant women who have early sepsis show a salutary response with crystalloid and antimicrobial therapy, and if indicated, debridement of infected tissue. Conversely, if hypotension is not corrected following vigorous fluid infusion, then the prognosis is more guarded. At this juncture, if there also is no response to β-adrenergic inotropic agents, this indicates severe and unresponsive extracellular fluid extravasation with vascular insufficiency, overwhelming myocardial depression, or both. Oliguria and continued peripheral vasoconstriction characterize a secondary, cold phase of septic shock that is rarely survived. Another poor prognostic sign is continued renal, pulmonary, and cerebral dysfunction once hypotension has been corrected (Angus, 2013). The average risk of death increases by 15 to 20 percent with failure of each organ system. With three systems, mortality rates are 70 percent (Martin, 2003; Wheeler, 1999).

image Management

In 2004 an internationally directed consensus effort was launched as the Surviving Sepsis Campaign (Dellinger, 2008). The cornerstone of management is early goal-directed management, and it stresses prompt recognition of serious bacterial infection and close monitoring of vital signs and urine flow. Institution of this protocol has improved survival rates (Angus, 2013; Barochia, 2010).

An algorithm for management of sepsis syndrome is shown in Figure 47-6. The three basic steps are performed as simultaneously as possible and include evaluation of the sepsis source and its sequelae, cardiopulmonary function assessment, and immediate management. The most important step in sepsis management is rapid infusion of 2 L and sometimes as many as 4 to 6 L of crystalloid fluids to restore renal perfusion in severely affected women (Vincent, 2013). Simultaneously, appropriately chosen broad-spectrum antimicrobials are begun. There is hemoconcentration because of the capillary leak. Thus, if anemia coexists with severe sepsis, then blood is given along with crystalloid to maintain the hematocrit at approximately 30 percent (Munford, 2012; Rivers, 2001). The use of colloid solution such as hetastarch is controversial, and we as well as others do not recommend its use (Angus, 2013; Ware, 2000). Indeed, a recent Scandinavian randomized trial comparing hydroxyethyl starch and Ringer acetate reported a higher mortality rate with the starch solution (Perner, 2012). Another recent study found equivalent results with 6-percent hydroxyethyl starch compared with normal saline (Myburgh, 2012). In vasopressor-dependent shock, some recommend albumin infusions (Angus, 2013; Vincent, 2013).


FIGURE 47-6 Algorithm for evaluation and management of sepsis syndrome. Rapid and aggressive implementation is paramount for success. The three steps—Evaluate, Assess, and Manage—are carried out as simultaneously as possible.

Aggressive volume replacement ideally is promptly followed by urinary output of at least 30 and preferably 50 mL/hr, as well as other indicators of improved perfusion. If not, then consideration is given for vasoactive drug therapy. Mortality rates are high when sepsis is further complicated by respiratory or renal failure. With severe sepsis, damage to pulmonary capillary endothelium and alveolar epithelium causes alveolar flooding and pulmonary edema. This may occur even with low or normal pulmonary capillary wedge pressures, as with the acute respiratory distress syndrome discussed on page 943 and depicted in Figure 47-1.

Broad-spectrum antimicrobials are chosen empirically based on the source of infection. They are given promptly in maximal doses after appropriate cultures are taken of blood, urine, or exudates not contaminated by normal flora. In severe sepsis, appropriate empirical coverage results in better survival rates (Barochia, 2010; MacArthur, 2004). Acute pyelonephritis is usually caused by Enterobacteriaceae as discussed in Chapter 53 (p. 1054). For pelvic infections, empirical coverage with regimens such as ampicillin plus gentamicin plus clindamycin generally suffices (Chap. 37p. 685). Associated incisional and other soft-tissue infections are increasingly likely to be caused by methicillin-resistant S aureus, thus vancomycin therapy is added (Klevens, 2007; Rotas, 2007). With a septic abortion, a Gram-stained smear may be helpful in identifying Clostridium perfringens or group A streptococcal organisms. This is also true for deep fascial infections.

Surgical Treatment

Continuing sepsis may prove fatal, and debridement of necrotic tissue or drainage of purulent material is crucial (Angus, 2013; Mabie, 1997). In obstetrics, the major causes of sepsis are infected abortion, pyelonephritis, and puerperal pelvic infections that include infection of perineal lacerations or of hysterotomy or laparotomy incisions. With an infected abortion, uterine contents must be removed promptly by curettage as described in Chapter 18 (p. 356). Hysterectomy is seldom indicated unless gangrene has resulted.

For women with pyelonephritis, continuing sepsis should prompt a search for obstruction caused by calculi or by a perinephric or intrarenal phlegmon or abscess. Renal sonography or “one-shot” pyelography may be used to diagnose obstruction and calculi. Computed tomography (CT) may be helpful to identify a phlegmon or abscess. With obstruction, ureteral catheterization, percutaneous nephrostomy, or flank exploration may be lifesaving (Chap. 53p. 1057).

Most cases of puerperal pelvic sepsis are clinically manifested in the first several days postpartum, and intravenous antimicrobial therapy without tissue debridement is generally curative. There are several exceptions. First is massive uterine myonecrosis caused by group A β-hemolytic streptococcal or clostridial infections (Soper, 2011; Sugiyama, 2010; Yamada, 2010). Those with early-onset disease have presenting findings listed in Table 47-6. The mortality rate in these women with gangrene as shown in Figure 47-7 is high, and prompt hysterectomy may be lifesaving (Mabie, 1997; Nathan, 1993). Group A β-hemolytic streptococci and clostridial colonization or infection also cause toxic-shock syndrome without obvious gangrene as reviewed by Mason and Aronoff (2012). These are due to either streptococcal toxic-shock syndrome-like toxin or clostridial exotoxin that evolved from S aureus (Chap. 37p. 690). In many of these cases, there is bacteremia and widespread tissue invasion, but an intact uterus and abdominal incisions. If uterine necrosis can be excluded—usually by CT scanning—then in our experiences, as well as in others, hysterectomy may not be necessary (Soper, 2011). Still, these infections are highly lethal (Yamada, 2010).

TABLE 47-6. Clinical Findings in 55 Women with Group A β-Hemolytic Infection Manifest within 12 Hours of Delivery



FIGURE 47-7 A fatal case of group A β-hemolytic Streptococcus pyogenes puerperal infection following an uncomplicated vaginal delivery at term. The infection caused uterine gangrene and overwhelming sepsis syndrome. Arrows point to overtly “ballooned-out” black gangrenous areas of the postpartum uterus at the time of laparotomy for hysterectomy.

A second exception is necrotizing fasciitis of the episiotomy site or abdominal surgical incision. As described by Gallup and coworkers (2002), these infections are a surgical emergency and are aggressively managed as discussed in Chapter 37 (p. 686).

Third, persistent or aggressive uterine infection with necrosis, uterine incision dehiscence, and severe peritonitis may lead to sepsis (Chap. 37p. 688). Thus, women following cesarean delivery who are suspected of having peritonitis should be carefully evaluated for uterine incisional necrosis or bowel perforation. These infections tend to be less aggressive than necrotizing group A streptococcal infections and develop later postpartum. CT imaging of the abdomen and pelvis can frequently determine if either of these has eventuated. If either is suspected, then prompt surgical exploration is indicated. With incisional necrosis, hysterectomy is usually necessary (Fig. 37-4p. 688). Last, peritonitis and sepsis much less commonly may result from a ruptured parametrial, intraabdominal, or ovarian abscess (Chap. 37p. 687).

Adjunctive Therapy

Vasoactive Drugs and Corticosteroids. As shown in Figure 47-6, a septic woman is supported with continuing crystalloid infusion, blood transfusions, and ventilation. In some cases, other measures may be necessary. Of options, vasoactive drugs are not given unless aggressive fluid treatment fails to correct hypotension and perfusion abnormalities. First-line vasopressors are norepinephrine, epinephrine, dopamine, dobutamine, or phenylephrine (Vincent, 2013). Low-dose vasopressin combined with norepinephrine infusion did not improve survival (Russell, 2008).

The use of corticosteroids remains controversial. Serum cortisol levels are typically elevated in sepsis, and higher levels are associated with increased mortality rates (Sam, 2004). Some but not all studies show a salutary effect of corticosteroid administration. It is thought that critical illness-related corticosteroid insufficiencyCIRCI—may play a role in recalcitrant hypotension. Thus, corticosteroids may be considered for use in vasopressor-dependent patients (Angus, 2013; Dellinger, 2008).

Coagulopathy. Endotoxin stimulates endothelial cells to upregulate tissue factor and thus procoagulant production (Chap. 41p. 808). At the same time, it decreases the anticoagulant action of activated protein C. Several agents developed to block coagulation, however, did not improve outcomes—some include antithrombin III, platelet-activating factor antagonist, and tissue factor pathway inhibitor (Abraham, 2003; Suffredini, 2011; Warren, 2001). A 10-year dalliance with recombinant activated protein C—drotrecogin alfa—followed after results of an early trial were promising. However, subsequent randomized trials have shown no survival benefits (Ranieri, 2012; Wenzel, 2012). Experience with its use in pregnancy had been limited to case reports (Eppert, 2011; Gupta, 2011; Medve, 2005).

Other Therapies. There are several other therapies that have proven ineffective. Some of these include antiendotoxin antibody and E5 murine monoclonal IgM antiendotoxin antibody; anticytokine antibodiesto IL-1TNF-α, and bradykinin; and a nitric oxide synthase inhibitor (Munford, 2012; Russell, 2006).


Traumatic injuries such as homicide and similar violent events are a leading cause of death in young women. Depending on definitions used, up to 20 percent of pregnant women suffer physical trauma (American College of Obstetricians and Gynecologists, 2010; Romero, 2012). Injury-related deaths are the most commonly identified nonobstetrical cause of maternal mortality (Brown, 2009; Horon, 2001). In a California study of 4.8 million pregnancies, almost 1 in 350 women were hospitalized for injuries from assaults (El Kady, 2005). In an audit from Parkland Hospital, motor vehicle accidents and falls accounted for 85 percent of injuries sustained by 1682 pregnant women (Hawkins, 2007). Homicides and suicides are also a major cause of pregnancy-associated deaths (Lin, 2011; Shadigian, 2005). From the National Violent Death Reporting System, Palladino and colleagues (2011) found that there were 2.0 pregnancy-associated suicides per 100,000 live births. The rate was 2.9 per 100,000 for pregnancy-associated homicides. And interrelated, intimate partner violence may be linked to these suicides (Martin, 2007).

image Blunt Trauma

Physical Abuse—Intimate Partner Violence

According to the United States Department of Justice (2013), women aged 16 to 24 years have the highest per capita rates of intimate partner violence—19.4 per 1000. As many as 10 million women each year are physically assaulted, sexually assaulted, or stalked by an intimate partner (Centers for Disease Control and Prevention, 2013a). One goal in violence prevention for Healthy People 2010 was the reduction of physical abuse directed at women by male partners. The Pregnancy Risk Assessment Monitoring Systems—PRAMS—report showed some improvement in these areas (Suellentrop, 2006).

Even more appalling is that physical violence directed at women continues during pregnancy. Most data have been accrued by public institutions, and abuse rates range from 1 to 20 percent during pregnancy (American College of Obstetricians and Gynecologists, 2011b). In Phoenix, more than 13 percent of women who enrolled for prenatal services had a history of physical or sexual abuse (Coonrod, 2007). Abuse is linked to poverty, poor education, and use of tobacco, alcohol, and illicit drugs (Centers for Disease Control and Prevention, 2008). Unfortunately, abused women tend to remain with their abusers, and the major risk factor for intimate partner homicide is prior domestic violence (Campbell, 2007). Finally, women seeking pregnancy termination have a higher incidence of intimate partner violence (Bourassa, 2007).

The woman who is physically abused tends to present late, if at all, for prenatal care. In the study cited above, pregnant women hospitalized in California as a result of assault had significantly increased perinatal morbidity rates (El Kady, 2005). Immediate sequelae included uterine rupture, preterm delivery, and maternal and perinatal death. Subsequent outcomes included increased rates of placental abruption, preterm and low-birthweight infants, and other adverse outcomes. Silverman and associates (2006) reported similar results from PRAMS, which included more than 118,000 pregnancies in 26 states. Others have cited increased preterm birth and depression (Rodriguez, 2008).

Preventatively, the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2012) recommend universal screening for intimate partner violence at the initial prenatal visit, during each trimester, and again at the postpartum visit (Chap. 9p. 174). Others recommend a case-finding approach based on clinical suspicion (Robertson-Blackmore, 2013; Wathen, 2003).

Sexual Assault

According to the Centers for Disease Control and Prevention (2012), 20 percent of adult women will be sexually assaulted sometime during their lives. More than 90 percent of the nearly 200,000 rape victims in the United States in 2006 were women; 80 percent were younger than 30 years; and 44 percent were younger than 18. Satin and coworkers (1992) reviewed more than 5700 female sexual assault victims in Dallas County and reported that 2 percent were pregnant. Associated physical trauma is common (Sugar, 2004). From a forensic standpoint, evidence collection protocol is not altered (Linden, 2011).

In addition to attention to physical injuries, exposure to sexually transmitted diseases must be considered. The Centers for Disease Control and Prevention (2010) recommends antimicrobial prophylaxis against gonorrhea, chlamydial infection, and trichomoniasis (Table 47-7). If the woman is not pregnant, another very important aspect is emergency contraception, as recommended by the American College of Obstetricians and Gynecologists (2012) and discussed in detail in Chapter 38 (p. 714).

TABLE 47-7. Guidelines for Prophylaxis against Sexually Transmitted Disease in Victims of Sexual Assault


The importance of psychological counseling for the rape victim and her family cannot be overemphasized. There is a 30- to 35-percent lifetime risk each for posttraumatic stress disorder, major depression, and suicide contemplation (Linden, 2011).

Automobile Accidents

At least 3 percent of pregnant women are involved in motor vehicle accidents each year in the United States. Using data from PRAMS, Sirin and colleagues (2007) estimated that 92,500 pregnant women are injured annually. Motor-vehicle crashes are the most common causes of serious, life-threatening, or fatal blunt trauma during pregnancy (Brown, 2009; Luley, 2013; Patteson, 2007; Vladutiu, 2013). Mattox and Goetzl (2005) report these accidents to be the leading cause of traumatic fetal deaths as well, and this was also true for Parkland Hospital (Hawkins, 2007). As with all motor vehicle crashes, alcohol use is commonly associated. But sadly, as many as half of accidents occur without seat-belt use, and many of these deaths would likely be preventable by the three-point restraints shown in Figure 47-8 (Klinich, 2008; Luley, 2013; Metz, 2006). Seat belts prevent contact with the steering wheel, and they reduce abdominal impact pressure (Motozawa, 2010).


FIGURE 47-8 Illustration showing correct use of three-point automobile restraint. The upper belt is above the uterus, and the lower belt fits snugly across the upper thighs and well below the uterus.

Original concerns regarding injuries caused by airbag deployment have been somewhat allayed (Matsushita, 2014). One study included 30 such women from 20 to 37 weeks’ gestation whose airbag deployed in accidents with a median speed of 35 mph (Metz, 2006). A third were not using seat belts, and there was one fetal death from the single case of placental abruption. Almost 75 percent had contractions, half had abdominal pain, and in 20 percent, there were abnormal fetal heart rate tracings. In a retrospective cohort study that included 2207 pregnant women in crashes with airbag deployment, perinatal outcomes were not clinically different from 1141 controls without airbags (Schiff, 2010). Importantly, 96 percent of both groups used seat belts.

Other Blunt Trauma

Some other common causes of blunt trauma are falls and aggravated assaults. In the California review reported by El Kady and associates (2005), intentionally inflicted injuries were present in approximately a third of pregnant women who were hospitalized for trauma. Less common are blast or crush injury (Sela, 2008). With blunt trauma, there can be serious intraabdominal injuries. Even so, bowel injuries are less frequent because of the protective effect of a large uterus. Still, diaphragmatic, splenic, liver, and kidney injuries may also be sustained. Particularly worrisome is the specter of amnionic-fluid embolism, which has been reported with even mild trauma (Ellingsen, 2007; Pluymakers, 2007). Retroperitoneal hemorrhage is possibly more common than in nonpregnant women (Takehana, 2011).

Orthopedic injuries are also encountered with some regularity (Desai, 2007). From the Parkland Hospital trauma unit, 6 percent of 1682 pregnant women evaluated had orthopedic injuries. This subset was also at increased risk for placental abruption, preterm delivery, and perinatal mortality (Cannada, 2008). In a review of 101 pelvic fractures during pregnancy, there was a 9-percent maternal and 35-percent fetal mortality rate (Leggon, 2002). In another study of pelvic and acetabular fractures during 15 pregnancies, there was one maternal death, and four of 16 fetuses died (Almog, 2007). Finally, head trauma and neurosurgical care raise unique issues (Qaiser, 2007).

Fetal Injury and Death

Perinatal death rates increase with the severity of maternal injuries. Fetal death is more likely with direct fetoplacental injury, maternal shock, pelvic fracture, maternal head injury, or hypoxia (Ikossi, 2005; Pearlman, 2008). Motor vehicle accidents caused 82 percent of fetal deaths from trauma. Death was caused by placental injury in half, and by uterine rupture in 4 percent (Weiss, 2001). Patteson and coworkers (2007) reported similar findings.

Although uncommon, fetal skull and brain injuries are more likely if the head is engaged and the maternal pelvis is fractured (Palmer, 1994). Conversely, fetal head injuries, presumably from a contrecoup effect, may be sustained in unengaged vertex or nonvertex presentations. Fetal skull fractures are rare and best seen using CT imaging (Sadro, 2012). Sequelae include intracranial hemorrhage (Green-Thompson, 2005). A newborn with paraplegia and contractures associated with a motor vehicle accident sustained several months before birth was described by Weyerts and colleagues (1992). Other injuries have included fetal decapitation or incomplete midabdominal fetal transection at midpregnancy (Rowe, 1996; Weir, 2008).

Placental Injuries—Abruption or Tear

Catastrophic events that occur with blunt trauma include placental injuries—abruption or placental tear or “fracture”—and uterine rupture (Fig. 47-9 and 47-10). Placental separation from trauma is likely caused by deformation of the elastic myometrium around the relatively inelastic placenta (Crosby, 1968). This may result from a deceleration injury as the large uterus meets the immovable steering wheel or seat belt. Some degree of abruption complicates 1 to 6 percent of “minor” injuries and up to 50 percent of “major” injuries (Pearlman, 1990; Schiff, 2002). Abruption was found to be more likely if vehicle speed exceeded 30 mph (Reis, 2000).


FIGURE 47-9 Acute deceleration injury occurs when the elastic uterus meets the steering wheel. As the uterus stretches, the inelastic placenta shears from the decidua basalis. Intrauterine pressures as high as 550 mm Hg are generated.


FIGURE 47-10 Mechanism of placental tear or “fracture” caused by a deformation-reformation injury. Placental abruption is seen as blood collecting in the retroplacental space. Inset. From here, blood can be forced into placental bed venules and enter maternal circulation. Such maternofetal hemorrhage may be identified with Kleihauer-Betke testing.

Clinical findings with traumatic abruption may be similar to those for spontaneous placental abruption (Chap. 41p. 796). Kettel and coworkers (1988) emphasized that traumatic abruption may be occult and unaccompanied by uterine pain, tenderness, or bleeding. Stettler and associates (1992) reviewed our experiences with 13 such women at Parkland Hospital. Of these, 11 had uterine tenderness, but only five had vaginal bleeding. Because traumatic abruption is more likely to be concealed and generate higher intrauterine pressures, associated coagulopathy is more likely than with nontraumatic abruption. Partial separation may also generate uterine activity as described more fully on page 955. Other features are evidence of fetal compromise such as fetal tachycardia, late decelerations, and acidosis and fetal death.

If there is considerable abdominal force associated with trauma, then the placenta can be torn, or “fractured” (see Fig. 47-10). If so, then life-threatening fetal hemorrhage may be encountered either into the amnionic sac or by fetomaternal hemorrhage (Pritchard, 1991). The tear is linear or stellate such as shown in Figure 47-11 and is caused by rapid deformation and reformation. Especially if there is ABO compatibility, fetomaternal hemorrhage is quantified using a Kleihauer-Betke stain of maternal blood (see Fig. 47-11). A small amount of fetal-maternal bleeding has been described in up to a third of trauma cases, and in 90 percent of these, the volume is < 15 mL (Goodwin, 1990; Pearlman, 1990). Nontraumatic placental abruption is much less often associated with significant fetomaternal hemorrhage because there usually is only minimal fetal bleeding into the intervillous space. With traumatic abruption, however, massive fetomaternal hemorrhage may coexist (Stettler, 1992). In one study there was a 20-fold risk of associated uterine contractions and preterm labor if there is evidence for a fetomaternal bleed (Muench, 2004).


FIGURE 47-11 A. Partial placental abruption in which the adherent blood clot has been removed. Note the laceration of the placenta (arrow), which caused fetal death from massive fetomaternal hemorrhage. B. Kleihauer–Betke stain of a peripheral smear of maternal blood. The dark cells that constituted 4.5 percent of red blood cells are fetal in origin, whereas the empty cells are maternal.

Uterine Rupture

Blunt trauma results in uterine rupture in < 1 percent of severe cases (American College of Obstetricians and Gynecologists, 2010). Rupture is more likely in a previously scarred uterus and is usually associated with a direct impact of substantial force. Decelerative forces following a 25-mph collision can generate up to 500 mm Hg of intrauterine pressure in a properly restrained woman (Crosby, 1968). Clinical findings may be identical to those for placental abruption with an intact uterus, and maternal and fetal deterioration are soon inevitable. Pearlman and Cunningham (1996) described uterine fundal “blowout” with fetal decapitation in a 20-week pregnancy following a high-speed collision. Similarly, Weir and colleagues (2008) described supracervical uterine avulsion and fetal transection at 22 weeks. CT scanning may be useful to diagnose uterine rupture with a dead fetus or placental separation (Kopelman, 2013; Manriquez, 2010; Sadro, 2012; Takehana, 2011).

image Penetrating Trauma

In a study of 321 pregnant women with abdominal trauma, Petrone (2011) reported a 9-percent incidence of penetrating injuries—77 percent were gunshot wounds and 23 percent were stab wounds. The incidence of maternal visceral injury with penetrating trauma is only 15 to 40 percent compared with 80 to 90 percent in nonpregnant individuals (Stone, 1999). When the uterus sustains penetrating wounds, the fetus is more likely than the mother to be seriously injured. Indeed, although the fetus sustains injury in two thirds of cases with penetrating uterine injuries, maternal visceral injuries are seen in only 20 percent. Still, their seriousness is underscored in that maternal-fetal mortality rates are significantly higher than those seen with blunt abdominal injuries in pregnancy. Specifically, maternal mortality was 7 versus 2 percent, and fetal mortality was 73 versus 10 percent, respectively.

image Management of Trauma

Maternal and fetal outcomes are directly related to the severity of injury. That said, commonly used methods of severity scoring do not take into account significant morbidity and mortality rates related to placental abruption and thus to pregnancy outcomes. In a study of 582 pregnant women hospitalized for injuries, the injury severity score did not accurately predict adverse pregnancy outcomes (Schiff, 2005). Importantly, relatively minor injuries were associated with preterm labor and placental abruption. Others have reached similar conclusions (Biester, 1997; Ikossi, 2005). In a study of 317 pregnant women at 24 weeks’ gestation or more who had “minor trauma,” 14 percent had clinically significant uterine contractions requiring extended fetal evaluation past 4 hours (Cahill, 2008).

With few exceptions, treatment priorities in injured pregnant women are directed as they would be in nonpregnant patients (Barraco, 2010; Mirza, 2010). Primary goals are evaluation and stabilization of maternal injuries. Attention to fetal assessment during the acute evaluation may divert attention from life-threatening maternal injuries (American College of Obstetricians and Gynecologists, 2010; Brown, 2009). Basic rules of resuscitation include ventilation, arrest of hemorrhage, and treatment of hypovolemia with crystalloid and blood products. Importantly, the large uterus is positioned off the great vessels to diminish its affect on vessel compression and decreased cardiac output.

Following emergency resuscitation, evaluation is continued for fractures, internal injuries, bleeding sites, and placental, uterine, and fetal trauma. Radiography is not proscribed, but special attention is given to indications. One report observed that pregnant trauma victims had less radiation exposure than nonpregnant controls (Ylagan, 2008). Brown and colleagues (2005) advocated screening abdominal sonography followed by CT scanning for positive sonographic findings. Procedures used include the FAST scan—focused assessment with sonography for trauma. This is a 5-minute, four- to six-view imaging study that evaluates perihepatic, perisplenic, pelvic, and pericardial views (Rose, 2004). In general, if fluid is seen in any of these views, then the volume is > 500 mL. However, this amount has not been corroborated for pregnancy. In some cases, open peritoneal lavage may be informative (Tsuei, 2006).

Penetrating injuries in most cases must be evaluated using radiography. Because clinical response to peritoneal irritation is blunted during pregnancy, an aggressive approach to exploratory laparotomy is pursued. Whereas exploration is mandatory for abdominal gunshot wounds, some clinicians advocate close observation for selected stab wounds. Diagnostic laparoscopy has also been used (Chap. 46p. 928).

Cesarean Delivery

The necessity for cesarean delivery of a live fetus depends on several factors. Laparotomy itself is not an indication for hysterotomy. Some considerations include gestational age, fetal condition, extent of uterine injury, and whether the large uterus hinders adequate treatment or evaluation of other intraabdominal injuries (Tsuei, 2006).

Electronic Monitoring

As for many other acute or chronic maternal conditions, fetal well-being may reflect the status of the mother. Thus, fetal monitoring is another “vital sign” that helps to evaluate the extent of maternal injuries. Even if the mother is stable, electronic monitoring may suggest placental abruption. In a study by Pearlman and coworkers (1990), no woman had an abruption if uterine contractions were less often than every 10 minutes within the 4 hours after trauma was sustained. Almost 20 percent of women who had contractions more frequently than every 10 minutes in the first 4 hours had an associated placental abruption. In these cases, abnormal tracings were common and included fetal tachycardia and late decelerations. Conversely, no adverse outcomes were reported in women who had normal monitor tracings (Connolly, 1997). Importantly, if tocolytics are used for these contractions, they may obfuscate findings, and we do not recommend them.

Because placental abruption usually develops early following trauma, fetal monitoring is begun as soon as the mother is stabilized. The ideal duration of posttrauma monitoring is not precisely known. From data cited above, observation for 4 hours is reasonable with a normal tracing and no other sentinel findings such as contractions, uterine tenderness, or bleeding. Certainly, monitoring should be continued as long as there are uterine contractions, nonreassuring fetal heart patterns, vaginal bleeding, uterine tenderness or irritability, serious maternal injury, or ruptured membranes (American College of Obstetricians and Gynecologists, 2010). In rare cases, placental abruption has developed days after trauma (Higgins, 1984).

Fetal-Maternal Hemorrhage

It is unclear whether routine use of the Kleihauer-Betke or an equivalent test in pregnant trauma victims might modify adverse outcomes associated with fetal anemia, cardiac arrhythmias, and death (Pak, 1998). In a retrospective review of 125 pregnant women with blunt injuries, the Kleihauer-Betke test was reported to have a sensitivity of 56 percent, a specificity of 71 percent, and an accuracy of 27 percent (Towery, 1993). These investigators concluded that the test was of little value during acute trauma management. They also concluded that electronic fetal monitoring or sonography or both were more useful in detecting fetal or pregnancy-associated complications than the Kleihauer-Betke test. Others have reached similar conclusions, although a positive test with fetal cells of 0.1 percent was predictive of uterine contractions or preterm labor (Connolly, 1997; Muench, 2003, 2004).

For the woman who is D-negative, administration of anti-D immunoglobulin should be considered. This may be omitted if a test for fetal bleeding is negative. Even with anti-D immunoglobulin, alloimmunization may still develop if the fetal-maternal hemorrhage exceeds 15 mL of fetal cells (Chap. 15p. 311).

Another important aspect of care for the pregnant trauma patient is to ensure that her tetanus immunization is current. When indicated, a dose of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine (Tdap) is preferred for its neonatal pertussis immunity benefits described in Chapter 9 (p. 184) (Centers for Disease Control and Prevention, 2013b). If unavailable, tetanus toxoid (TT) or tetanus and diphtheria toxoids (Td) are suitable alternatives.


Treatment of burned pregnant women is similar to that for nonpregnant patients (Pacheco, 2005). With treatment, it is generally agreed that pregnancy does not alter maternal outcome from thermal injury compared with that of nonpregnant women of similar age. As perhaps expected, maternal and fetal survival parallels the percentage of burned surface area. Karimi and colleagues (2009) reported higher mortality rates for both with suicidal attempts and with inhalational injuries. The composite mortality for more than 200 women from six studies increased in a linear fashion as the percent body-surface area burned increased (Fig. 47-12). For 20-, 40-, and 60-percent burns, the maternal mortality rates were approximately 4, 30, and 93 percent, respectively. The corresponding fetal mortality rates were 20, 48, and 96 percent, respectively. With severe burns, the woman usually enters labor spontaneously within a few days to a week and often delivers a stillborn. Contributory factors are hypovolemia, pulmonary injury, septicemia, and the intensely catabolic state associated with these burns (Radosevich, 2013).


FIGURE 47-12 Maternal and fetal mortality rates by burn severity in 211 women. (Data from Akhtar, 1994; Amy, 1985; Mabrouk, 1977; Maghsoudi, 2006; Rayburn, 1984; Rode, 1990.)

Following serious abdominal burns, skin contractures that develop may be painful during a subsequent pregnancy and may even require surgical decompression and split-skin autografts (Matthews, 1982; Widgerow, 1991). In a follow-up study of seven women with severe circumferential truncal burns sustained at a mean age of 7.7 years, all of 14 subsequent pregnancies were delivered at term without major complications (McCauley, 1991). Loss or distortion of nipples may cause problems in breast feeding (Fig. 47-13). Interestingly, normal abdominal tissue expansion due to pregnancy appears to be an excellent source for obtaining skin grafts postpartum to correct scar deformities at other body sites (Del Frari, 2004).


FIGURE 47-13 This 22-year-old nullipara sustained severe burns at age 12 years, and massive scarring followed. Both breasts were replaced by scar tissue. Following delivery, a few drops of colostrum were expressed from the left nipple, but no breast engorgement was noted. (Photograph contributed by Drs. A. R. Mahale and A. P. Sakhare, Maharashtra, India.)

image Electrical and Lightning Injuries

Earlier case reports suggested a high fetal mortality rate with electric shock (Fatovich, 1993). In a prospective cohort study, however, Einarson and coworkers (1997) showed similar perinatal outcomes in 31 injured women compared with those of noninjured controls. They concluded that traditional 110-volt North American electrical current likely is less dangerous than 220-volt currents available in Europe. A woman with iliofemoral thrombosis at 29 weeks’ gestation that may have been related to a mild electrical shock at 22 weeks was described (Sozen, 2004). Thermal burns may be extensive and require expert wound care.

The pathophysiological effects of lightning injuries can be devastating. García Gutiérrez and associates (2005) reviewed 12 case reports of injuries during pregnancy and added their own.


Cardiac arrest is rare during pregnancy. General topics regarding planning and equipment have been reviewed by the American College of Obstetricians and Gynecologists (2011a). There are special considerations for cardiopulmonary resuscitation (CPR) conducted in the second half of pregnancy, and these are outlined in the American Heart Association 2010 guidelines (Vanden Hoek, 2010). The committee acknowledges the following as standards for critically ill pregnant women: (1) relieve possible vena caval compression by left lateral uterine displacement, (2) administer 100-percent oxygen, (3) establish intravenous access above the diaphragm, (4) assess for hypotension that warrants therapy, which is defined as systolic blood pressure < 100 mmHg or < 80 percent of baseline, and (5) review possible causes of critical illness and treat conditions as early as possible.

In nonpregnant women, external chest compression results in a cardiac output approximately 30 percent of normal. In late pregnancy, this may be even less with CPR because of uterine aortocaval compression (Clark, 1997). Thus, it is paramount to accompany other resuscitative efforts with uterine displacement. Displacement can be accomplished by tilting the operating table laterally, by placing a wedge under the right hip—an example is the Cardiff resuscitation wedge, or by pushing the uterus to the left manually (Rees, 1988). If no equipment is available, such as in an out-of-hospital arrest, an individual may kneel on the floor with the maternal back on his or her thighs to form a “human wedge” (Whitty, 2002).

image Cesarean Delivery

During maternal resuscitation, because of pregnancy-induced hindrances on CPR efforts, emergent perimortem cesarean delivery for fetal salvage and improved maternal resuscitation may be considered (Vanden Hoek, 2010). Some have stated that cesarean delivery is indicated with 4 to 5 minutes of beginning CPR if the fetus is viable (Moise, 1997). There is an undeniably inverse correlation between neurologically intact neonatal survival and the cardiac arrest-to-delivery interval in women delivered by perimortem cesarean (Katz, 2012). Specifically, of newborns delivered within 5 minutes of arrest, 98 percent are neurologically intact; within 6 to 15 minutes, 83 percent are intact; within 16 to 25 minutes, 33 percent are intact; and within 26 to 35 minutes, only 25 percent are intact (Clark, 1997). This, coupled with some evidence that delivery may also enhance maternal resuscitation, has led the American College of Obstetricians and Gynecologists (2011a) to recommend consideration for cesarean delivery within 4 minutes of cardiac arrest in these cases.

This serious and sometimes contentious issue is far from evidence based. To wit, Katz and associates (2005) reviewed 38 perimortem cesarean deliveries with a “large selection bias.” They concluded that these reports supported—but “fell far from proving”—that perimortem cesarean delivery within 4 minutes of maternal cardiac arrest improves maternal and fetal outcomes. Even so, as emphasized by Clark and coworkers (1997), and in our experiences, these goals rarely can be met in actual practice. For example, most cases of cardiac arrest occur in uncontrolled circumstances, and thus, the time to CPR initiation alone would exceed the first 5 minutes. Thus “crash” cesarean delivery would supersede resuscitative efforts, be necessarily done without appropriate anesthesia or surgical equipment, and more likely than not, would lead to maternal death. Moreover, the distinction between a perimortem versus postmortem cesarean operation is imperative (Katz, 2012). Last, in the balance, any choice may favor survival of the mother over the fetus, or vice versa, and thus there are immediate unresolvable ethical concerns. Katz (2012) has recently provided a scholarly review of perimortem cesarean delivery.

image Maternal Brain Death

Occasionally, a pregnant woman with a supposedly healthy intact fetus will be kept on somatic support to await fetal viability or maturity. This is discussed in Chapter 60 (p. 1199).

image Envenomation

According to their review, Brown and colleagues (2013) reported that clinically significant envenomations in pregnant women are from snakes, spiders, scorpions, jellyfish, and hymenoptera such as bees, wasps, hornets, and ants. Adverse outcomes are related to maternal effects. They conclude that limited evidence supports the use of a venom-specific approach that includes symptomatic care, antivenom administration when appropriate, anaphylaxis treatment, and fetal assessment.


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